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Respiration: ventilation
Physiology
Respiration: ventilation
is separated from the circulation by the blood–brain barrier, which is largely impermeable to H+ and hydrogen carbonate (HCO3), but freely permeable to CO2. This movement of CO2 into CSF leads to a rise in CSF H+ (exaggerated due to low CSF protein levels, leading to a low buffering capacity). The subsequent rise in H+ leads to the stimulation of the receptors and rise in respiratory rate mentioned earlier. A compensatory rise in CSF bicarbonate ions (HCO3−) will occur over a few days, thus reducing the respiratory drive of a high arterial CO2 (as for patients with long-standing hypercapnoea). Peripheral sensors are primarily concerned with sensing changes in the partial pressure of arterial oxygen (PaO2). Their excision leads to loss of hypoxic ventilatory drive. They are located above and below the aortic arch (aortic bodies) and at the bifurcation of the common carotid arteries (carotid bodies). The carotid bodies in particular have a very high blood flow (2 litre/100 g tissue) and can thus respond to alterations in arterial PaO2. A decrease in PaO2 leads to an increase in alveolar ventilation (Figure 1). Reduction in PaO2 below normal (13.3 KPa) elicits a small increase in chemoreceptor discharge until PaO2 falls to approximately 8 KPa. Further reduction in PaO2 below 8 KPa elicits a powerful increase in chemoreceptor discharge. The carotid bodies also produce a response to changes in pH and the partial pressure of arterial carbon dioxide (PaCO2), albeit to a lesser degree than the central receptors. Pulmonary stretch receptors are located within airway smooth muscle and may inhibit respiration when stimulated by lung distension. Irritant receptors are located within the airway epithelium. Responses include bronchoconstriction and coughing. J-receptors are located in alveolar walls, near capillaries, and are affected by interstitial disease and possibly pulmonary vascular engorgement. Joint and muscle receptors – limb movement may stimulate ventilation during exercise.
Mark Holliday Upma Misra
Abstract The process of external respiration involves the uptake of oxygen and excretion of carbon dioxide in the lungs by means of ventilation and gas transfer. Ventilation is controlled by neural and chemical regulatory mechanisms, and ventilation changes in response to hypoxia and changes in acid-base balance. The most important muscle for inspiration is the diaphragm with abdominal wall muscles being the most important muscles of expiration. The work of breathing is required to move the lungs and chest wall and facilitate flow of gas through the airways. Resistance to flow of gas through the airway depends on the type of flow: laminar, turbulent or transitional. The compliance curve of the lung explains why ventilation is better at the base of the lungs compared with the apex. Dynamic compression of airways is a feature of forced expiration in healthy individuals; however, it may occur at low expiratory flow rates in certain lung diseases and thus limit exercise tolerance.
Keywords compliance; dynamic airway compression; lung mechanics; respiration; ventilation; work of breathing
Control of ventilation The physiological control mechanisms of ventilation consist of sensors and effectors, which are driven by the central nervous system to provide integrated patterns of response. The origin of respiratory control is outside the scope of this article and is covered elsewhere (Anaesthesia & Intensive Care Medicine 9: 437–40). Here, we recap the control of ventilation and then discuss in detail the mechanics.
Effectors Effectors are the muscles of respiration. In quiet breathing ins piration is active and expiration passive, becoming active with forced respiration. Inspiratory muscles – the diaphragm is the most important muscle of inspiration. Controlled by the phrenic nerve, the
Sensors Central sensors are the most important for immediate control of ventilation. They are located just beneath the ventral surface of the medulla proximate to cranial nerves IX and X. An increase in hydrogen ions (H+) or carbon dioxide (CO2) around these receptors leads to an increase in respiratory rate within seconds. The receptors lie in the extracellular fluid, the constitution of which is largely due to the surrounding cerebrospinal fluid (CSF). This fluid
Alveolar ventilation
Effect of arterial PaO2 on alveolar ventilation
Mark Holliday, MRCP, FRCA, is a Specialist Registrar in Anaesthesia and Intensive care in the Northern Deanery and is presently based at Sunderland Royal Hospital, Sunderland, UK. Conflicts of interest: none declared.
Normal PaCO2 PaO2
Upma Misra, FRCA, is a Consultant Anaesthetist at Sunderland Royal Hospital, Sunderland, UK. Conflicts of interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 10:3
High PaCO2
Figure 1
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© 2009 Elsevier Ltd. All rights reserved.
Physiology
s timulation of the diaphragm leads to contraction and flattening, depression of the abdominal contents and lifting of the ribs up and out. This movement is 1–2 cm in quiet breathing but can be up to 10 cm. The external intercostal muscles supplied by intercostals nerves also aid inspiration by the upward and forward movement of the ribs. This is often described as the ‘bucket handle’ movement of the ribs, which results in an increase in the lateral diameter of the chest. Contraction of the external intercostal muscles will aid inspiration, as will the accessory muscles of inspiration, which comprise the scalene muscles (elevate the first and second ribs) and the sterno mastoid muscles (raise the sternum). Expiratory muscles – expiration in quiet breathing is passive due to the elastic recoil of lungs and chest wall following active inspiration. Active expiration involves the abdominal muscles primarily but also the internal intercostals.
Mechanics of ventilation Work of breathing: ventilation requires the movement of the lung, chest wall and flow of gas through the airways. The effort to do this constitutes the work of breathing. Figure 3 illustrates this in terms of pressure and volume. Most of the work is done to overcome elastic forces, represented in Figure 3 by the hatched area. The energy consumed during inspiration is stored in the now stretched elastic structures. Additional work is then required to overcome airway and tissue resistance, represented by the green area in Figure 3. The work required to overcome airway resistance on expiration (blue area) is contained within the hatched area and is therefore provided by the energy stored during inspiration. This reinforces our knowledge that expiration is normally passive. However, during high-effort breathing the green and blue areas increase greatly and expiration becomes an active process.
Maintaining homeostasis
Elastic properties of the lung: the tendency of the lung is to collapse inward; this must be overcome to allow ventilation. Compliance is the unit volume change per unit pressure change. Compliance is altered by the elastic properties of the lung. A reduction in compliance (less volume change for given pressure change) occurs with an increase in fibrous tissue, engorgement of pulmonary vasculature, alveolar oedema/consolidation or collapse. A rise in compliance (increase volume change for given pressure change) occurs with normal aging and pulmonary emphysema (due in part to loss of resistive elastic tissues). Surface tension is a major factor in compliance. Surface tension is measured in Dynes, and is the force acting across a figurative line on the surface of a liquid. It is caused by the greater attraction of adjacent liquid molecules for each other than the surrounding gas molecules. In a sphere this tension leads to a pressure that tends to collapse the sphere. Laplace’s law describes this inward pressure (P): P = 4 T/r, where T is surface tension and r the radius (in the lung this is modified to P = 2 T/r). Alveoli can be thought of as thin-walled fluid-lined spheres, and so to expand alveoli, and hence the lung, this collapsing pressure must be overcome. It is advantageous if this pressure is minimized. Surfactant is a phospholipid, an important constituent of which is dipalmitoyl phosphatidylcholine (DPPC). This constituent is synthesized within the lung by type II pneumocytes. Production develops late in fetal life. The addition of surfactant to a liquid lowers the surface tension. This occurs because of the make-up of the DPPC molecule. It is hydrophobic at one end and hydrophilic at the other. Because of the alignment of the molecules on the fluid surface the normal attractive forces between liquid molecules are opposed. Lower surface tension increases compliance and reduces the work required for inspiration. The effect of surface tension means that small spheres tend to collapse more than larger ones. In the lung these ‘spheres’ (alveoli) are linked by the small airways and this tendency would lead to small alveoli collapsing, inflating adjacent larger alveoli. Surfactant reduces this deleterious action as it leads to smaller spheres having a greater reduction in surface tension. Transduction of fluid in to the alveoli is reduced and thus alveoli are kept dry. The respiratory disease seen in neonates born before the production of surfactant has begun illustrates the effect of the absence of surfactant.
We can now combine these aspects of ventilatory control to look at responses to alterations in PaCO2, PaO2 and pH. Carbon dioxide A rise in PaCO2 will stimulate respiration. Figure 2 illustrates the change in minute ventilation in response to a rise in arterial PaCO2. Very large changes in minute ventilation occur for very small rises in PaCO2. Also shown in Figure 2 is the enhanced response in the presence of hypoxia. This response may be affected by drugs such as opioids, sedatives, or by chronic hypercapnoea. In these cases the slope of the curve is shallower and the curve may move to the right. Oxygen Figure 1 shows the change in ventilation in response to change in PaO2 at differing PaCO2 levels. An exaggerated response to falling PaO2 can be seen in the presence of high PaCO2. At normal PaCO2, moderate hypoxia does not stimulate ventilation. In patients who have become chronically hypercapnic this response to hypoxia may become more important for resting respiratory drive. pH A falling arterial pH, even in the presence of normal PaCO2, will lead to increased ventilation.
Effect of arterial PaCO2 on alveolar ventilation Low PaO2 Alveolar ventilation
Normal PaO2 High PaO2
PaCO2 Figure 2
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Physiology
and a number of other factors. For laminar flow, resistance is increased with length, rise in viscosity and dramatically increased by a reduction in radius. Transitional flow occurs primarily at branches of tubes and with rising flow rates, and is a mixture of laminar and turbulent flow. In turbulent flow resistance is high when compared with laminar flow, but no simple formula exists to describe resistance in turbulent flow. However, it is worth noting that viscosity is unimportant, whereas increasing gas density increases resistance. Whether gas flow is laminar or turbulent depends on the Reynolds number. A Reynolds number above 2000 makes turbulent flow more likely. From the equations below we can see that the Reynolds number increases with a rise in radius, velocity and density, and a fall in viscosity. Applying these principles to the lung we see that turbulent flow is likely in the trachea, transitional flow throughout the bronchial tree (due to its rapidly branching nature) and laminar flow likely only in very small airways.
Work of breathing
Volume
Expiration
Inspiration
FRC Intra-pleural pressure Figure 3
Chest wall elasticity
Laminar flow
The chest wall has a tendency to spring outward. This persists up to volumes of 75% of vital capacity. In equilibrium this is balanced against the tendency of the lungs to collapse.
R=
8nl πr 4
where R is the resistance, n is the viscosity, l is the length and r is the radius.
Airway resistance
Reynolds number
Gas flow through tubes is laminar, turbulent or transitional. Resistance to flow is dependent on the type of flow in the airway
Re =
where Re is the Reynolds number, r is the radius, n is the viscosity, d is the density and v is the velocity. Applied resistance – resistance decreases as lung volume rises because airways are held open (increasing their radius) by expansion of surrounding lung tissue. At low volumes the converse is seen, and resistance increases. On applying the above equations it can be seen that airway narrowing (e.g. by swelling or smooth muscle constriction) will increase resistance. This increase in resistance increases the work of breathing on both inspiration and expiration.
Regional differences in ventilation 100
50
0 +10
0
–10
–20
Volume (% of maximal volume)
a
Regional differences in ventilation
–30
Ventilation is greater at the bases of the lung compared with the apex. This is explained by the compliance curve of the lung. At the beginning of inspiration the lung base is positioned at a lower part (lower volume at end expiration) of the curve and there is a correspondingly greater change in volume for unit pressure change. Whereas the apex is at a higher part of the curve (greater volume at end expiration) and therefore experiences a smaller volume change for the corresponding pressure change. The relative positions on the compliance curve of the base and apex, and their differing volumes at end expiration, can be explained by the effect of the weight of the lung itself, altering intra-pleural pressure. At very low lung volumes the basal intra-pleural pressure is above atmospheric pressure and the lung is compressed. As a consequence, ventilation on inspiration is reduced because part of the intra-pleural pressure change is taken up overcoming this compression. At these low
Intra-pleural pressure (cmH2O)
100
50
0 +10
0
–10
–20
Volume (% of maximal volume)
b
–30
Intra-pleural pressure (cmH2O) Figure 4 a Normal lung volumes; b very low lung volumes
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Physiology
lung volumes the apex is more advantageously placed on the compliance curve (Figure 4).
Dynamic airways compression End inspiration
Dynamic airways compression
0 Airway pressure
At mid and low lung volumes the peak expiratory flow rate is independent of the expiratory effort. At a certain point further increases in effort do not increase expiratory flow. The reason for this effect are summarized below and illustrated in Figure 5. At the end of inspiration there is a positive pressure holding the airways open. On active expiration the intra-pleural pressure and alveolar pressure increase similarly. The airway pressure decreases as expiration continues, this pressure drop is due to resistance to flow in the airways and a reduction in airway elastic support as lung volume falls. A point is reached when the airway pressure falls below intra-thoracic pressure, this results in compression of the airway and a limitation of flow. Further increasing the effort will not alter the airway/intra-thoracic pressure difference and will therefore not increase flow. The point at which this compression begins moves closer to the alveoli, and hence flow limitation is greater at low lung volumes, with increased airways resistance and with reduced lung elasticity and airway support, such as in emphysema. This flow limitation is seen in healthy individuals only in forced expiration but in disease states it may occur at expiratory flow rates low enough to cause a limitation of exercise capacity. ◆
0
Intra-pleural pressure (cmH2O)
0 –10
0
Forced expiration
+10
+20 +30 +20
Figure 5
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Respiration: ventilation
is separated from the circulation by the blood–brain barrier, which is largely impermeable to H+ and hydrogen carbonate (HCO3), but freely permeable to CO2. This movement of CO2 into CSF leads to a rise in CSF H+ (exaggerated due to low CSF protein levels, leading to a low buffering capacity). The subsequent rise in H+ leads to the stimulation of the receptors and rise in respiratory rate mentioned earlier. A compensatory rise in CSF bicarbonate ions (HCO3−) will occur over a few days, thus reducing the respiratory drive of a high arterial CO2 (as for patients with long-standing hypercapnoea). Peripheral sensors are primarily concerned with sensing changes in the partial pressure of arterial oxygen (PaO2). Their excision leads to loss of hypoxic ventilatory drive. They are located above and below the aortic arch (aortic bodies) and at the bifurcation of the common carotid arteries (carotid bodies). The carotid bodies in particular have a very high blood flow (2 litre/100 g tissue) and can thus respond to alterations in arterial PaO2. A decrease in PaO2 leads to an increase in alveolar ventilation (Figure 1). Reduction in PaO2 below normal (13.3 KPa) elicits a small increase in chemoreceptor discharge until PaO2 falls to approximately 8 KPa. Further reduction in PaO2 below 8 KPa elicits a powerful increase in chemoreceptor discharge. The carotid bodies also produce a response to changes in pH and the partial pressure of arterial carbon dioxide (PaCO2), albeit to a lesser degree than the central receptors. Pulmonary stretch receptors are located within airway smooth muscle and may inhibit respiration when stimulated by lung distension. Irritant receptors are located within the airway epithelium. Responses include bronchoconstriction and coughing. J-receptors are located in alveolar walls, near capillaries, and are affected by interstitial disease and possibly pulmonary vascular engorgement. Joint and muscle receptors – limb movement may stimulate ventilation during exercise.
Mark Holliday Upma Misra
Abstract The process of external respiration involves the uptake of oxygen and excretion of carbon dioxide in the lungs by means of ventilation and gas transfer. Ventilation is controlled by neural and chemical regulatory mechanisms, and ventilation changes in response to hypoxia and changes in acid-base balance. The most important muscle for inspiration is the diaphragm with abdominal wall muscles being the most important muscles of expiration. The work of breathing is required to move the lungs and chest wall and facilitate flow of gas through the airways. Resistance to flow of gas through the airway depends on the type of flow: laminar, turbulent or transitional. The compliance curve of the lung explains why ventilation is better at the base of the lungs compared with the apex. Dynamic compression of airways is a feature of forced expiration in healthy individuals; however, it may occur at low expiratory flow rates in certain lung diseases and thus limit exercise tolerance.
Keywords compliance; dynamic airway compression; lung mechanics; respiration; ventilation; work of breathing
Control of ventilation The physiological control mechanisms of ventilation consist of sensors and effectors, which are driven by the central nervous system to provide integrated patterns of response. The origin of respiratory control is outside the scope of this article and is covered elsewhere (Anaesthesia & Intensive Care Medicine 9: 437–40). Here, we recap the control of ventilation and then discuss in detail the mechanics.
Effectors Effectors are the muscles of respiration. In quiet breathing ins piration is active and expiration passive, becoming active with forced respiration. Inspiratory muscles – the diaphragm is the most important muscle of inspiration. Controlled by the phrenic nerve, the
Sensors Central sensors are the most important for immediate control of ventilation. They are located just beneath the ventral surface of the medulla proximate to cranial nerves IX and X. An increase in hydrogen ions (H+) or carbon dioxide (CO2) around these receptors leads to an increase in respiratory rate within seconds. The receptors lie in the extracellular fluid, the constitution of which is largely due to the surrounding cerebrospinal fluid (CSF). This fluid
Alveolar ventilation
Effect of arterial PaO2 on alveolar ventilation
Mark Holliday, MRCP, FRCA, is a Specialist Registrar in Anaesthesia and Intensive care in the Northern Deanery and is presently based at Sunderland Royal Hospital, Sunderland, UK. Conflicts of interest: none declared.
Normal PaCO2 PaO2
Upma Misra, FRCA, is a Consultant Anaesthetist at Sunderland Royal Hospital, Sunderland, UK. Conflicts of interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 10:3
High PaCO2
Figure 1
151
© 2009 Elsevier Ltd. All rights reserved.
Physiology
s timulation of the diaphragm leads to contraction and flattening, depression of the abdominal contents and lifting of the ribs up and out. This movement is 1–2 cm in quiet breathing but can be up to 10 cm. The external intercostal muscles supplied by intercostals nerves also aid inspiration by the upward and forward movement of the ribs. This is often described as the ‘bucket handle’ movement of the ribs, which results in an increase in the lateral diameter of the chest. Contraction of the external intercostal muscles will aid inspiration, as will the accessory muscles of inspiration, which comprise the scalene muscles (elevate the first and second ribs) and the sterno mastoid muscles (raise the sternum). Expiratory muscles – expiration in quiet breathing is passive due to the elastic recoil of lungs and chest wall following active inspiration. Active expiration involves the abdominal muscles primarily but also the internal intercostals.
Mechanics of ventilation Work of breathing: ventilation requires the movement of the lung, chest wall and flow of gas through the airways. The effort to do this constitutes the work of breathing. Figure 3 illustrates this in terms of pressure and volume. Most of the work is done to overcome elastic forces, represented in Figure 3 by the hatched area. The energy consumed during inspiration is stored in the now stretched elastic structures. Additional work is then required to overcome airway and tissue resistance, represented by the green area in Figure 3. The work required to overcome airway resistance on expiration (blue area) is contained within the hatched area and is therefore provided by the energy stored during inspiration. This reinforces our knowledge that expiration is normally passive. However, during high-effort breathing the green and blue areas increase greatly and expiration becomes an active process.
Maintaining homeostasis
Elastic properties of the lung: the tendency of the lung is to collapse inward; this must be overcome to allow ventilation. Compliance is the unit volume change per unit pressure change. Compliance is altered by the elastic properties of the lung. A reduction in compliance (less volume change for given pressure change) occurs with an increase in fibrous tissue, engorgement of pulmonary vasculature, alveolar oedema/consolidation or collapse. A rise in compliance (increase volume change for given pressure change) occurs with normal aging and pulmonary emphysema (due in part to loss of resistive elastic tissues). Surface tension is a major factor in compliance. Surface tension is measured in Dynes, and is the force acting across a figurative line on the surface of a liquid. It is caused by the greater attraction of adjacent liquid molecules for each other than the surrounding gas molecules. In a sphere this tension leads to a pressure that tends to collapse the sphere. Laplace’s law describes this inward pressure (P): P = 4 T/r, where T is surface tension and r the radius (in the lung this is modified to P = 2 T/r). Alveoli can be thought of as thin-walled fluid-lined spheres, and so to expand alveoli, and hence the lung, this collapsing pressure must be overcome. It is advantageous if this pressure is minimized. Surfactant is a phospholipid, an important constituent of which is dipalmitoyl phosphatidylcholine (DPPC). This constituent is synthesized within the lung by type II pneumocytes. Production develops late in fetal life. The addition of surfactant to a liquid lowers the surface tension. This occurs because of the make-up of the DPPC molecule. It is hydrophobic at one end and hydrophilic at the other. Because of the alignment of the molecules on the fluid surface the normal attractive forces between liquid molecules are opposed. Lower surface tension increases compliance and reduces the work required for inspiration. The effect of surface tension means that small spheres tend to collapse more than larger ones. In the lung these ‘spheres’ (alveoli) are linked by the small airways and this tendency would lead to small alveoli collapsing, inflating adjacent larger alveoli. Surfactant reduces this deleterious action as it leads to smaller spheres having a greater reduction in surface tension. Transduction of fluid in to the alveoli is reduced and thus alveoli are kept dry. The respiratory disease seen in neonates born before the production of surfactant has begun illustrates the effect of the absence of surfactant.
We can now combine these aspects of ventilatory control to look at responses to alterations in PaCO2, PaO2 and pH. Carbon dioxide A rise in PaCO2 will stimulate respiration. Figure 2 illustrates the change in minute ventilation in response to a rise in arterial PaCO2. Very large changes in minute ventilation occur for very small rises in PaCO2. Also shown in Figure 2 is the enhanced response in the presence of hypoxia. This response may be affected by drugs such as opioids, sedatives, or by chronic hypercapnoea. In these cases the slope of the curve is shallower and the curve may move to the right. Oxygen Figure 1 shows the change in ventilation in response to change in PaO2 at differing PaCO2 levels. An exaggerated response to falling PaO2 can be seen in the presence of high PaCO2. At normal PaCO2, moderate hypoxia does not stimulate ventilation. In patients who have become chronically hypercapnic this response to hypoxia may become more important for resting respiratory drive. pH A falling arterial pH, even in the presence of normal PaCO2, will lead to increased ventilation.
Effect of arterial PaCO2 on alveolar ventilation Low PaO2 Alveolar ventilation
Normal PaO2 High PaO2
PaCO2 Figure 2
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Physiology
and a number of other factors. For laminar flow, resistance is increased with length, rise in viscosity and dramatically increased by a reduction in radius. Transitional flow occurs primarily at branches of tubes and with rising flow rates, and is a mixture of laminar and turbulent flow. In turbulent flow resistance is high when compared with laminar flow, but no simple formula exists to describe resistance in turbulent flow. However, it is worth noting that viscosity is unimportant, whereas increasing gas density increases resistance. Whether gas flow is laminar or turbulent depends on the Reynolds number. A Reynolds number above 2000 makes turbulent flow more likely. From the equations below we can see that the Reynolds number increases with a rise in radius, velocity and density, and a fall in viscosity. Applying these principles to the lung we see that turbulent flow is likely in the trachea, transitional flow throughout the bronchial tree (due to its rapidly branching nature) and laminar flow likely only in very small airways.
Work of breathing
Volume
Expiration
Inspiration
FRC Intra-pleural pressure Figure 3
Chest wall elasticity
Laminar flow
The chest wall has a tendency to spring outward. This persists up to volumes of 75% of vital capacity. In equilibrium this is balanced against the tendency of the lungs to collapse.
R=
8nl πr 4
where R is the resistance, n is the viscosity, l is the length and r is the radius.
Airway resistance
Reynolds number
Gas flow through tubes is laminar, turbulent or transitional. Resistance to flow is dependent on the type of flow in the airway
Re =
where Re is the Reynolds number, r is the radius, n is the viscosity, d is the density and v is the velocity. Applied resistance – resistance decreases as lung volume rises because airways are held open (increasing their radius) by expansion of surrounding lung tissue. At low volumes the converse is seen, and resistance increases. On applying the above equations it can be seen that airway narrowing (e.g. by swelling or smooth muscle constriction) will increase resistance. This increase in resistance increases the work of breathing on both inspiration and expiration.
Regional differences in ventilation 100
50
0 +10
0
–10
–20
Volume (% of maximal volume)
a
Regional differences in ventilation
–30
Ventilation is greater at the bases of the lung compared with the apex. This is explained by the compliance curve of the lung. At the beginning of inspiration the lung base is positioned at a lower part (lower volume at end expiration) of the curve and there is a correspondingly greater change in volume for unit pressure change. Whereas the apex is at a higher part of the curve (greater volume at end expiration) and therefore experiences a smaller volume change for the corresponding pressure change. The relative positions on the compliance curve of the base and apex, and their differing volumes at end expiration, can be explained by the effect of the weight of the lung itself, altering intra-pleural pressure. At very low lung volumes the basal intra-pleural pressure is above atmospheric pressure and the lung is compressed. As a consequence, ventilation on inspiration is reduced because part of the intra-pleural pressure change is taken up overcoming this compression. At these low
Intra-pleural pressure (cmH2O)
100
50
0 +10
0
–10
–20
Volume (% of maximal volume)
b
–30
Intra-pleural pressure (cmH2O) Figure 4 a Normal lung volumes; b very low lung volumes
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Physiology
lung volumes the apex is more advantageously placed on the compliance curve (Figure 4).
Dynamic airways compression End inspiration
Dynamic airways compression
0 Airway pressure
At mid and low lung volumes the peak expiratory flow rate is independent of the expiratory effort. At a certain point further increases in effort do not increase expiratory flow. The reason for this effect are summarized below and illustrated in Figure 5. At the end of inspiration there is a positive pressure holding the airways open. On active expiration the intra-pleural pressure and alveolar pressure increase similarly. The airway pressure decreases as expiration continues, this pressure drop is due to resistance to flow in the airways and a reduction in airway elastic support as lung volume falls. A point is reached when the airway pressure falls below intra-thoracic pressure, this results in compression of the airway and a limitation of flow. Further increasing the effort will not alter the airway/intra-thoracic pressure difference and will therefore not increase flow. The point at which this compression begins moves closer to the alveoli, and hence flow limitation is greater at low lung volumes, with increased airways resistance and with reduced lung elasticity and airway support, such as in emphysema. This flow limitation is seen in healthy individuals only in forced expiration but in disease states it may occur at expiratory flow rates low enough to cause a limitation of exercise capacity. ◆
0
Intra-pleural pressure (cmH2O)
0 –10
0
Forced expiration
+10
+20 +30 +20
Figure 5
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